67 research outputs found
Production of phi mesons at mid-rapidity in sqrt(s_NN) = 200 GeV Au+Au collisions at RHIC
We present the first results of meson production in the K^+K^- decay channel
from Au+Au collisions at sqrt(s_NN) = 200 GeV as measured at mid-rapidity by
the PHENIX detector at RHIC. Precision resonance centroid and width values are
extracted as a function of collision centrality. No significant variation from
the PDG accepted values is observed. The transverse mass spectra are fitted
with a linear exponential function for which the derived inverse slope
parameter is seen to be constant as a function of centrality. These data are
also fitted by a hydrodynamic model with the result that the freeze-out
temperature and the expansion velocity values are consistent with the values
previously derived from fitting single hadron inclusive data. As a function of
transverse momentum the collisions scaled peripheral.to.central yield ratio RCP
for the is comparable to that of pions rather than that of protons. This result
lends support to theoretical models which distinguish between baryons and
mesons instead of particle mass for explaining the anomalous proton yield.Comment: 326 authors, 24 pages text, 23 figures, 6 tables, RevTeX 4. To be
submitted to Physical Review C as a regular article. Plain text data tables
for the points plotted in figures for this and previous PHENIX publications
are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm
CYP1A1gene polymorphisms increase lung cancer risk in a high-incidence region of Spain: a case control study
Forty years literature review of primary lung lymphoma
There are several unresolved issues through out the literature regarding the entity of primary lung lymphoma. Extensive literature review of this uncommon pathology is carried out
Soy isoflavones, estrogen therapy, and breast cancer risk: analysis and commentary
There has been considerable investigation of the potential for soyfoods to reduce risk of cancer, and in particular cancer of the breast. Most interest in this relationship is because soyfoods are essentially a unique dietary source of isoflavones, compounds which bind to estrogen receptors and exhibit weak estrogen-like effects under certain experimental conditions. In recent years the relationship between soyfoods and breast cancer has become controversial because of concerns – based mostly on in vitro and rodent data – that isoflavones may stimulate the growth of existing estrogen-sensitive breast tumors. This controversy carries considerable public health significance because of the increasing popularity of soyfoods and the commercial availability of isoflavone supplements. In this analysis and commentary we attempt to outline current concerns regarding the estrogen-like effects of isoflavones in the breast focusing primarily on the clinical trial data and place these concerns in the context of recent evidence regarding estrogen therapy use in postmenopausal women. Overall, there is little clinical evidence to suggest that isoflavones will increase breast cancer risk in healthy women or worsen the prognosis of breast cancer patients. Although relatively limited research has been conducted, and the clinical trials often involved small numbers of subjects, there is no evidence that isoflavone intake increases breast tissue density in pre- or postmenopausal women or increases breast cell proliferation in postmenopausal women with or without a history of breast cancer. The epidemiologic data are generally consistent with the clinical data, showing no indication of increased risk. Furthermore, these clinical and epidemiologic data are consistent with what appears to be a low overall breast cancer risk associated with pharmacologic unopposed estrogen exposure in postmenopausal women. While more research is required to definitively allay concerns, the existing data should provide some degree of assurance that isoflavone exposure at levels consistent with historical Asian soyfood intake does not result in adverse stimulatory effects on breast tissue
J/psi production from proton-proton collisions at sqrt(s) = 200 GeV
J/psi production has been measured in proton-proton collisions at sqrt(s)=
200 GeV over a wide rapidity and transverse momentum range by the PHENIX
experiment at RHIC. Distributions of the rapidity and transverse momentum,
along with measurements of the mean transverse momentum and total production
cross section are presented and compared to available theoretical calculations.
The total J/psi cross section is 3.99 +/- 0.61(stat) +/- 0.58(sys) +/-
0.40(abs) micro barns. The mean transverse momentum is 1.80 +/- 0.23(stat) +/-
0.16(sys) GeV/c.Comment: 326 authors, 6 pages text, 4 figures, 1 table, RevTeX 4. To be
submitted to PRL. Plain text data tables for the points plotted in figures
for this and previous PHENIX publications are (or will be) publicly available
at http://www.phenix.bnl.gov/papers.htm
Measurement of Single Electron Event Anisotropy in Au+Au Collisions at sqrt(s_NN) = 200 GeV
The transverse momentum dependence of the azimuthal anisotropy parameter v_2,
the second harmonic of the azimuthal distribution, for electrons at
mid-rapidity (|eta| < 0.35) has been measured with the PHENIX detector in Au+Au
collisions at sqrt(s_NN) = 200 GeV. The measurement was made with respect to
the reaction plane defined at high rapidities (|eta| = 3.1 -- 3.9). From the
result we have measured the v_2 of electrons from heavy flavor decay after
subtraction of the v_2 of electrons from other sources such as photon
conversions and Dalitz decay from light neutral mesons. We observe a non-zero
single electron v_2 with a 90% confidence level in the intermediate p_T region.Comment: 330 authors, 11 pages text, RevTeX4, 9 figures, 1 tables. Submitted
to Physical Review C. Plain text data tables for the points plotted in
figures for this and previous PHENIX publications are (or will be) publicly
available at http://www.phenix.bnl.gov/papers.htm
Systematic Studies of the Centrality and sqrt(s_NN) Dependence of dE_T/deta and dN_ch/deta in Heavy Ion Collisions at Mid-rapidity
The PHENIX experiment at RHIC has measured transverse energy and charged
particle multiplicity at mid-rapidity in Au+Au collisions at sqrt(s_NN) = 19.6,
130 and 200 GeV as a function of centrality. The presented results are compared
to measurements from other RHIC experiments, and experiments at lower energies.
The sqrt(s_NN) dependence of dE_T/deta and dN_ch/deta per pair of participants
is consistent with logarithmic scaling for the most central events. The
centrality dependence of dE_T/deta and dN_ch/deta is similar at all measured
incident energies. At RHIC energies the ratio of transverse energy per charged
particle was found independent of centrality and growing slowly with
sqrt(s_NN). A survey of comparisons between the data and available theoretical
models is also presented.Comment: 327 authors, 25 pages text, 19 figures, 17 tables, RevTeX 4. To be
submitted to Physical Review C as a regular article. Plain text data tables
for the points plotted in figures for this and previous PHENIX publications
are (or will be) publicly available at http://www.phenix.bnl.gov/papers.htm
Centrality Dependence of Charm Production from Single Electrons in Au+Au Collisions at sqrt(s_NN) = 200 GeV
The PHENIX experiment has measured mid-rapidity transverse momentum spectra
(0.4 < p_T < 4.0 GeV/c) of single electrons as a function of centrality in
Au+Au collisions at sqrt(s_NN) = 200 GeV. Contributions to the raw spectra from
photon conversions and Dalitz decays of light neutral mesons are measured by
introducing a thin (1.7% X_0) converter into the PHENIX acceptance and are
statistically removed. The subtracted ``non-photonic'' electron spectra are
primarily due to the semi-leptonic decays of hadrons containing heavy quarks
(charm and bottom). For all centralities, charm production is found to scale
with the nuclear overlap function, T_AA. For minimum-bias collisions the charm
cross section per binary collision is N_cc^bar/T_AA = 622 +/- 57 (stat.) +/-
160 (sys.) microbarns.Comment: 326 authors, 4 pages text, 3 figures, 1 table, RevTeX 4. To be
submitted to Physical Review Letters. Plain text data tables for the points
plotted in figures for this and previous PHENIX publications are (or will be)
publicly available at http://www.phenix.bnl.gov/papers.htm
All-trans retinoic acid synergizes with topotecan to suppress AML cells via promoting RARα-mediated DNA damage
Epithelial cancers in the post-genomic era: should we reconsider our lifestyle?
The age-related epithelial cancers of the breast, colorectum and prostate are the most prevalent and are increasing in our aging populations. Epithelial cells turnover rapidly and mutations naturally accumulate throughout life. Most epithelial cancers arise from this normal mutation rate. All elderly individuals will harbour many cells with the requisite mutations and most will develop occult neoplastic lesions. Although essential for initiation, these mutations are not sufficient for the progression of cancer to a life-threatening disease. This progression appears to be dependent on context: the tissue ecosystem within individuals and lifestyle exposures across populations of individuals. Together, this implies that the seeds may be plentiful but they only germinate in the right soil. The incidence of these cancers is much lower in Eastern countries but is increasing with Westernisation and increases more acutely in migrants to the West. A Western lifestyle is strongly associated with perturbed metabolism, as evidenced by the epidemics of obesity and diabetes: this may also provide the setting enabling the progression of epithelial cancers. Epidemiology has indicated that metabolic biomarkers are prospectively associated with cancer incidence and prognosis. Furthermore, within cancer research, there has been a rediscovery that a switch in cell metabolism is critical for cancer progression but this is set within the metabolic status of the host. The seed may only germinate if the soil is fertile. This perspective brings together the different avenues of investigation implicating the role that metabolism may play within the context of post-genomic concepts of cancer
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